Previous work by the principal investigator has provided strong suggestive evidence that dopamine acts in the retina as a neurotransmitter which has inhibitory function. In addition a pilot study suggested that total depletion of retinal dopamine caused almost complete abolition of electro-retinographic flicker suppression. The implication was that dopamine may be involved in the neural mechanisms which account for rapid adaptation of the retina of light. It is proposed to deplete retinal dopamine by intraocular injection of reserpine and to measure the resultant effect on ERG flicker suppression. Subsequent measurements will be repeated after administration of DOPA and again after administration of DOPA following DOPA-decarboxylase inhibition. A similar series of measurements will be made at intervals following an attempt to destroy dopaminergic retinal fibers by intraocular injections of OH 6-OH-dopamine, in hopes of confirming an effect specifically mediated by the dopaminergic fibers. The potency of the catecholamines as pharmacologic agents is well know, and dopamine in the retina, if it is proven to have inhibitory transmitter function, may provide a pharmacologic handle for chemical and possibly therapeutic manipulation of retinal function.